The objective of this project was to develop biological tests for the early detection of lung damage that eventually results in pneumoconiosis in dust exposed miners. It specifically proposed to evaluate the relative balance between mediators of lung injury and their specific inhibitors which occur naturally and are thought to be altered in the dust diseases. Eleven nonsmoking controls and eleven currently dust-exposed miners underwent bronchoalveolar lavage in a subsegment of the right middle lobe. Cells were enumerated as to type (macrophages, lymphocytes, neutrophils) and viability. Fluid was analyzed for baseline values of superoxide dismutase (SOD), a scavenger of toxic superoxide ions. Alveolar macrophages were incubated with nothing, coal, silica or zymosan particles for 12 hours and the fluids analyzed for the release of (SOD), for the release of hydrogen peroxidase (H2O2), and glutathione peroxidase (GSH). We found that baseline IL-1B in our miners was significantly higher than in the controls. Alveolar macrophage IL-1B production in controls was not significantly increased after incubation with coal, silica or zymosan. IL-1B production in miners could not be further stimulated after incubation with coal, silica or zymosan. Although dust exposed miners had elevated levels of baseline IL-1B, neither miners nor controls alveolar macrophages could be stimulated to release more IL-1B on exposure to coal, silica or zymosan.